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Antiarrhythmic effects of interleukin 1 inhibition after myocardial infarction.

Abstract：

BACKGROUND:Interleukin 1β (IL-1β) is a key regulator of the inflammatory response after myocardial infarction (MI) by modulating immune cell recruitment, cytokine production, and extracellular matrix turnover. Elevated levels of IL-1β are associated with adverse remodeling, and inhibition of IL-1 signaling after MI results in improved contractile function. OBJECTIVE:The goal of this study was to determine whether IL-1 signaling also contributes to post-MI arrhythmogenesis. METHODS:MI was created in 2 murine models of elevated inflammation: atherosclerotic on the Western diet or wild-type with a subseptic dose of lipopolysaccharide. The role of IL-1β was assessed with the IL-1 receptor antagonist anakinra (10 mg/(kg·d), starting 24 hours post-MI). RESULTS:In vivo and ex vivo molecular imaging showed reduced myocardial inflammation after a 4-day course of anakinra treatment, despite no change in infarct size. At day 5 post-MI, high-speed optical mapping of transmembrane potential and intracellular Ca2+ in isolated hearts revealed that IL-1β inhibition improved conduction velocity, reduced action potential duration dispersion, improved intracellular Ca2+ handling, decreased transmembrane potential and Ca2+ alternans magnitude, and reduced spontaneous and inducible ventricular arrhythmias. These functional improvements were linked to increased expression of connexin 43 and sarcoplasmic reticulum Ca2+-ATPase. CONCLUSION:This study revealed a novel mechanism for IL-1β in contributing to defective excitation-contraction coupling and arrhythmogenesis in the post-MI heart. Our results suggest that inhibition of IL-1 signaling post-MI may represent a novel antiarrhythmic therapy.

journal_name

Heart Rhythm

journal_title

Heart rhythm

authors

De Jesus NM,Wang L,Lai J,Rigor RR,Francis Stuart SD,Bers DM,Lindsey ML,Ripplinger CM

doi

10.1016/j.hrthm.2017.01.027

subject

Has Abstract

pub_date

2017-05-01 00:00:00

pages

727-736

issue

5

eissn

1547-5271

issn

1556-3871

pii

S1547-5271(17)30077-2

journal_volume

14

pub_type

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